One Mutation, Two Diseases in Family with Ataxin-2 Expansion
Expansions in ataxin-2 can lead to either ALS or spinocerebellar ataxia—even in the same family, according to a new pedigree from New York.
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Expansions in ataxin-2 can lead to either ALS or spinocerebellar ataxia—even in the same family, according to a new pedigree from New York.
Two studies examine factors that heighten the risk for dementia in type 2 diabetes patients. Both highlight depression as a dangerous comorbidity.
Studies support the idea that mitochondrial changes drive aging and AD pathogenesis.
A stem cell-derived structure mimics crucial features of human brain development and could aid studies in schizophrenia, autism, maybe neurodegeneration.
Functional genomics and mouse analyses blame waning levels of histone-binding protein for memory loss in aging.
Researchers say that analyzing long stretches of homozygosity in people of Caribbean Hispanic descent represents an approach to finding rare, recessive Alzheimer’s mutations.
In sporadic and familial Parkinson's, faulty parkin may damage dopamine neurons by letting a deadly protein linger.
Researchers nabbed rare variants in Alzheimer’s genes by sequencing DNA from people with very high or very low levels of cerebrospinal fluid biomarkers.
Fueling (or rekindling) controversy over anti-aging benefits of sirtuins, researchers report that Sirt1 lengthens lifespan in mice.
Without the protein beclin 1, rapacious microglia choke on amyloid β.
As heat shock protein and co-chaperone team up to shield tau from degradation, they create toxic oligomers.
The insoluble proteome from Alzheimer’s brains points to RNA processing proteins as a novel component of aggregates.
New research connects extracellular Aβ to intracellular kinases that mediate its toxicity.
Older people improved memory and attention after playing a challenging video game, supporting the idea that multitasking could have benefits for cognition.
New imaging data suggests degeneration of the fornix could help identify seniors on the verge of cognitive decline.
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